YIC-C8-434
YIC-C8-434 is an orally active ACAT inhibitor. YIC-C8-434 selectively blocks cholesterol esterification in intestinal epithelial cells and hepatocytes without affecting the production of triglycerides or phospholipids. YIC-C8-434 effectively reduces intracellular cholesteryl ester levels and induces an increase in lipid droplet volume, exhibiting excellent cholesterol-lowering activity and safety. YIC-C8-434 disrupts the assembly of hepatitis C virus (HCV) virions, reduces HCV RNA synthesis and viral particle release. YIC-C8-434 can be used in studies related to hepatitis C virus infection.
For research use only. We do not sell to patients.
- Formula: C31H44N2O4
- Molecular Weight:508.69
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
In Vitro
YIC-C8-434 inhibits ACAT activity in Caco2 cell microsomes with an IC50 of 63 nM[1].
YIC-C8-434 inhibits ACAT activity in HepG2 cell microsomes with an IC50 of 88 nM[1].
YIC-C8-434 (10-20 μM; 29 h) decreases the number of lipid droplets and increases their average size in Huh-7 cells[2].
YIC-C8-434 (10-20 μM; 29 h) causes a modest reduction in HCV RNA synthesis but significantly impairs assembly of infectious JFH1 HCV virions in Huh-7 cells, reducing both extracellular and intracellular virus titers by approximately 5-fold[2].
YIC-C8-434 (10-20 μM; 29 h) does not reduce the abundance of HCV proteins (core, NS5A, E2, NS3) or the lipid droplet-associated cellular protein PLIN2 in JFH1 HCV-infected Huh-7 cells[2].
YIC-C8-434 (10 μM; 29 h) does not alter the co-localization of HCV core protein with lipid droplet-associated PLIN2 or with HCV RNA replication sites in JFH1 HCV-infected Huh-7 cells[2].
YIC-C8-434 (10-20 μM; 29 h) increases the buoyant density of released JFH1 HCV virions but does not reduce their specific infectivity, while decreasing overall extracellular viral particle release in Huh-7 cells[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:Huh-7
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Concentration:10, 20 μM
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Incubation Time:29 h
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Result:Caused a significant decrease in the number of lipid droplets (LDs) per cell compared to mock-treated cells.
Increased average LD size to twice that of mock-treated cells, with some LDs up to 3 times larger.
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Cell Line:JFH1 genotype 2a HCV-infected Huh-7
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Concentration:10, 20 μM
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Incubation Time:29 h
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Result:Caused a modest, less marked reduction in HCV RNA levels compared to triacsin C.
Significantly lowered extracellular infectious virus titers.
Decreased intracellular infectious virus TCID50 values by about 5-fold relative to mock-treated cells.
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Cell Line:JFH1 genotype 2a HCV-infected Huh-7
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Concentration:10, 20 μM
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Incubation Time:29 h
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Result:Had very little effect on the abundance of PLIN2, HCV core, NS5A, E2, or NS3 proteins compared to DMSO-treated cells.
Detected no significant reductions in targeted protein levels.
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Cell Line:JFH1 genotype 2a HCV-infected Huh-7
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Concentration:10 μM
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Incubation Time:29 h
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Result:Did not reduce the signal intensity for PLIN2 or core.
Maintained co-localization of PLIN2 and core at the same extent as in DMSO-treated cells (Pearson correlation coefficient of 0.60).
Preserved co-localization or close proximity of dsRNA punctate replication sites to core, similar to DMSO-treated cells.
In Vivo
YIC-C8-434 (10-100 mg/kg/d; p.o.; daily; 7 days) significantly inhibits hepatic VLDL cholesterol secretion in normal male Sprague-Dawley rats at an oral dose of 100 mg/kg/d, without affecting triacylglycerol or phospholipid secretion[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Sprague-Dawley (male, 120-150 g, hypercholesterolemia model via 0.5% cholic acid, 10% sucrose, 10% coconut oil diet)[1]
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Dosage:8.3 mg/kg/d; 17.2 mg/kg/d; 33.2 mg/kg/d
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Administration:p.o.; daily; 7 days
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Result:Reduced cholesterol absorption from 67.7% (control) to 56.1%, a 17% inhibition (p<0.01).
Reduced cholesterol absorption to 50.7% (p<0.01).
Reduced cholesterol absorption to 48.9% (p<0.01).
Chemical Information
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Molecular Weight 508.69
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Formula C31H44N2O4
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SMILES
COC1=CC(/C=C/C(N2CCN(CC2)C3=CC(C)=C(C)C=C3)=O)=CC(OC)=C1OCCCCCCCC
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Research Protocol for Infectious Diseases
Infectious-disease experiments test how pathogens interact with host barriers, innate immune receptors, inflammatory signaling, pathogen replication, and tissue injury; pattern-recognition receptors such as TLRs, RIG-I-like receptors, NOD-like receptors, and inflammasomes detect microbial molecules and activate NF-κB, interferon, and cytokine responses. The central hypothesis is that infection severity reflects the balance between pathogen burden and host response: protective inflammation restricts pathogen growth, whereas excessive or mislocalized inflammation contributes to tissue damage and disease phenotype. Unresolved questions include which host pathways are protective versus pathogenic, why some infection models fail to translate to human disease, and which combined readouts best predict clinically relevant infection outcomes.
Purity & Documentation
References
[1]. Ohishi K, et al. Inhibitory effects of N-(3,5-dimethoxy-4-n-octyloxycinnamoyl)-N'-(3,4-dimethylphenyl)piperazine (YIC-C8-434), an acyl-CoA:cholesterol O-acyltransferase inhibitor, on cholesterol esterification in the intestine and liver. Biological & pharmaceutical bulletin. 2003 Aug;26(8):1125-8. [Content Brief]
[2]. Liefhebber JM, et al. Modulation of triglyceride and cholesterol ester synthesis impairs assembly of infectious hepatitis C virus. The Journal of biological chemistry. 2014 Aug 01;289(31):21276-88. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
YIC-C8-434 Related Classifications
HY-138198A Related Classifications
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